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Salidroside attenuates interleukin‐1β‐induced inflammation in human osteoarthritis chondrocytes
Author(s) -
Zhang Yuan,
Zhao Qing
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.27076
Subject(s) - salidroside , nitric oxide , chemistry , nitric oxide synthase , inflammation , interleukin , pharmacology , prostaglandin e2 , matrix metalloproteinase , biochemistry , immunology , medicine , endocrinology , cytokine , organic chemistry
Salidroside, a bioactive constituent isolated from Rhodiola rosea , has been reported to have anti‐inflammatory effects. However, the effects of salidroside on interleukin (IL)‐1β‐stimulated osteoarthritis (OA) chondrocytes remain to be elucidated. Thus, this study aimed to evaluate the anti‐inflammatory effects of salidroside on IL‐1β‐stimulated human OA chondrocytes and explore its underlying mechanisms. Our results showed that salidroside significantly inhibited the production of nitric oxide and prostaglandin E‐2, as well as suppressed the expression of inducible nitric oxide synthase and cyclooxygenase‐2 in IL‐1β‐stimulated chondrocytes ( P < .05). In addition, salidroside also suppressed IL‐1β‐induced matrix metalloproteinases production in human OA chondrocytes ( P < .05). Furthermore, pretreatment with salidroside prevented IL‐1β‐induced NF‐κB activation in OA chondrocytes ( P < .05). In conclusion, the current study demonstrated that salidroside inhibited the IL‐1β‐induced inflammatory response in OA chondrocytes via inhibition of NF‐κB activation.